It has been shown that cGAMP (Cyclic 2'3'-GMP-AMP) is delivered via gap junction from cancer cells to adjacent astrocytes in metastatic brain tumors (BrM) and contributes to tumor progression. We aimed to reproduce the peritumoral astrocytic conditions by introducing cGAMP directly into astrocytes and to quantify the metabolic changes around the glutamine (Gln)-glutamate (Glu) cycle, as major CNS metabolism. In cGAMP-treated cells, the synthetic flux of Gln from ¹³C5,¹⁵N-Glu was reduced to about half that of control cells, while Glu secretory flux was increased two-fold. Furthermore, when Glu was evaluated as a chemoattractant for migration using HL60-derived neutrophils, which have been implicated in immunosuppression of BrM, exposure to 10-50 μM Glu tended to increase the migration. Downstream of the STING, which accepts cGAMP, a marked upregulation was observed for IL-6, CCL5, CCL2, CCL7, and CXCL1 by several tens of fold. They are target genes of the NF-κB pathway that may be involved in interferon activation as well as IRF3, and were completely suppressed by NF-κB blockage. Glu-induced oxidative stress has been reported to mediate activation of NF-κB. These results suggest that induction of NF-κB by cGAMP may be involved in Glu metabolic alterations, as well as in tumor microenvironment formation, including immune responses.